Physio git pathophysiology plus mc qs.


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Physio GIT pathophysiology plus MCQs.

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Physio git pathophysiology plus mc qs.

  1. 1. Gastrointestinal physiology Physiology of GIT disorders. Dr.M.A.M.Shaikhani.
  2. 2. <ul><li>Esophageal disorders: </li></ul><ul><li>Cause mainly dysphagia (difficult swallowing) as: </li></ul><ul><li>1.paralysis of 5 th , 9 th .& 10 th .cranial nerves. </li></ul><ul><li>2.poliomyelitis or encephalitis that destroy the swallowing center. </li></ul><ul><li>3.diseases of muscles (muscular dystrophy),neuromuscular diseases (myasthenia gravis) & botulism. </li></ul><ul><li>4.during recovery from general anesthesia or during coma,if vomiting occurs ,the vomitus will pass to the respiratory tract & lungs instead of passing outside the body through the mouth, because of failure of normal swallowing mechanisms specially the pharyngeal stage of swallowing. For this reason patients are advised to abstain from eating for at least 8 hours before surgery under general anesthesia. </li></ul><ul><li>5.Achalasia: Cogenital (sometimes acquired in Amer Trypanosomiasis) absence of myenteric plexus causing failure of receptive relaxation of LES, so dysphagia occurs & the eso. above the spastic segment dilates causing megaeso.& the treatment includes surgical or ballon dilatation or medical therapy in the form of nitrates,nifedipine or endoscopic intrasphincteric botulinium toxin injection. </li></ul>
  3. 3. <ul><li>Gastroduodenal disorders: </li></ul><ul><li>1.GASTRITIS : </li></ul><ul><li>Inflammation of gastric mucosa (gastritis): </li></ul><ul><li>Bacterial infection by Helicobacter Pylori . </li></ul><ul><li>Alcohol or NSAIDs as Aspirin </li></ul><ul><li>Antibodies against gastric cells (Adesonian Pernicious anemia). </li></ul><ul><li>Gastritis is specially common in elderly & may predispose to peptic ulceration of duodenum or stomach. </li></ul><ul><li>in autoimmune type( antibody-induced ) called Adesonian Pernicious anemia there is severe gastric atrophy which leads to loss of gastric acid(acholrhydria),intrinsic factor(essential for VB12 absorption) & pepsin all secreted by parietal cells so there will be megaloblastic anemia due to VB12 deficiency & pepsin deficiency causing loss of pepsin digestion in the stomach but the pancreatic proteolytic enzymes compensate for that & there will be no protein maldigestion. </li></ul>
  4. 4. <ul><li>2.Peptic ulceration(PU): </li></ul><ul><li>A defect in gastrointestinal mucosa(upper duodenum,stomach lesser curve,Lower Es ) due to imbalance between acid-pepsin luminal aggressive factors & mucosal defense mechanisms which include: </li></ul><ul><li>1.The bicarbonate rich mucous in duodenum& stomach. </li></ul><ul><li>2.The tight adjacent epithelial junctions. </li></ul><ul><li>3.The local blood flow & prostaglandin(PG) secretion. </li></ul><ul><li>4. Pancreatic bicarbonate secreted in response to Secretin secreted from upper intestinal cells in response to acid to neutralize excess acid coming from stomach. </li></ul><ul><li>5.Duodenal factors reducing gastric emptying as presence of duodenal irritation and acidity. </li></ul><ul><li>6.Feedback inhibition of gastric acid secretion by excess acid & inhibition of gastric acid-pepsin in the interdigestive period . </li></ul>
  5. 5. <ul><li>So peptic ulceration is caused either by : </li></ul><ul><li>A.Increased acid-pepsin secretion due to : </li></ul><ul><li>1.heriditary factors as peptic ulceration is common in some families. </li></ul><ul><li>2.Smoking. </li></ul><ul><li>3.Anxiety & emotional upset. </li></ul><ul><li>4.Tumours secreting gastrin as gastrinoma (Zollinger-Elison syndrome). </li></ul><ul><li>H Pylori. </li></ul><ul><li>B.Decreased mucosal defense mechanisms in: </li></ul><ul><li>1.Smoking by decreasing pancreatic HCO3 secretion. </li></ul><ul><li>2.Gastritis due to Helicobacter Pylori(HP). </li></ul><ul><li>3.NSAIDs use as aspirin which interfere with PGs secretion. </li></ul><ul><li>4.Irritation as alcohol. </li></ul><ul><li>5.Poor blood supply in burns & shock(stress ulcers). </li></ul>
  6. 6. <ul><li>Physiology of PU treatment: </li></ul><ul><li>A.Is either by decreasing acid secretion by: </li></ul><ul><li>1.drugs as antacids,H2-Blockers,anticholinergics,PGs,gastrin blockers,H+-K+ ATPase Blockers. </li></ul><ul><li>2.Surgery as vagatomy which is only needed if there is very aggressive ulcer or there are complications. </li></ul><ul><li>B.Or by increasing mucosal defense by: </li></ul><ul><li>1.Drugs which increase mucosal defense as sucralfate ,PGs,bismoth & carbinoxolone. </li></ul><ul><li>2.Treating HP infection by antibiotics. </li></ul>
  7. 7. <ul><li>Vomitig: </li></ul><ul><li>Is the process by which the GIT gets rid of overirritation, overdistention or overexcitation, which are transmitted by the vagi & sympathetic nerves to the vomiting center lying bilaterally in the medulla near the tractus solitarius at the level of dorsal motor nucleus of the vagus & the motor impulses that cause real vomiting act are transmitted from the vomiting center through the 5 th .,7 th .,9 th .,10 th .,& 12 th cranial nerves to the upper GIT & through the spinal nerves to the diaphragm & abdominal muscles . </li></ul><ul><li>The vomiting act is preceded by antiperistalsis which starts from the ileum to the duodenum causing backflow of SI contents to cause overdistention of duodenum& stomach , combined with contraction of abdominal muscles, diaphragm ,duodenum & stomach with relaxation of LES & opening of upper eso. Allows the vomitus to be thrown out. </li></ul>
  8. 8. <ul><li>Vomitig: </li></ul><ul><li>Another vomiting center in the brain outside the medullary vomiting center located bilaterally in floor of 4 th . Ventricle near the area postrema (chemoreceptor trigger zone CTZ) through which vomiting induced by some drugs (morphine ,apomorphine, cytotoxic drugs,digitalis derivatives)&motion sickness is mediated .CTZ causes vomiting by acting on the medullary vomiting center. </li></ul>
  9. 9. <ul><li>SI disorders : </li></ul><ul><li>Mainly is Malabsorption caused by many factors: </li></ul><ul><li>1.Pancreatic insufficiency due to chronic pancreatic or recurrent acute pancreatitis. </li></ul><ul><li>2.Biliary obstruction causing bile absence to contribute to fat digestion & absorption. </li></ul><ul><li>3.diseases of the villi due to celiac sprue in which there is sensitivity to gluten in the wheat & rye or tropical sprue in which there is bacterial infection of the villi or other diseases of the villi or giardiasis. </li></ul><ul><li>4.Lymphatic obstruction or diseases causing defective fat absorption. </li></ul><ul><li>In all these malabsorption disorders the first nutrient affected is fat causing steatorhea,then followed by protein,carbohydrates,vitamins malabsorption when the disease becomes more advanced. </li></ul>
  10. 10. <ul><li>Large intestine disorders: </li></ul><ul><li>Constipation: </li></ul><ul><li>Difficult passage of hard stool occurring when colonic movements are sluggish allowing absorption of large quantities of water.It occurs in: </li></ul><ul><li>1.Modern life style with frequent interference with normal colonic defecation reflexes. </li></ul><ul><li>2.Failure of bowel training in infancy. </li></ul><ul><li>3.Abuse of laxatives & enemas which interferes with normal defecation reflexes. </li></ul><ul><li>4.Emotional disturbances & anxiety causing (irritable bowel syndrome)manifested as alternating bowel habits with constipation followed by attacks of diarrhea. </li></ul><ul><li>5.Presence of tumours,strictures,adhesions,ulcers.So sudden change in bowel habits such as recent onset of constipation /or diarrhea should raise suspicion of serious disease as colon cancer. </li></ul><ul><li>6.Presense of aganglionic segment(absence of myenteric plexus) in the sigmoid colon causes formation of a spastic segment which leads to constipation & dilatation of colon above this segment causing megacolon. </li></ul>
  11. 11. <ul><li>7.Spinal cord injuries destroying defecation reflex which has 3 levels: </li></ul><ul><li>A.The myenteric plexus of sigmoid & colon. </li></ul><ul><li>B.The cord defecation reflex at the conus medularis of spinal cord. </li></ul><ul><li>C.Higher centers coordination of defecation above the level of conus medularis. </li></ul><ul><li>The destruction of conus medularis by spinal lesions or injuries at this level causes more severe disturbance of defecation requiring regular cathartics & enemas than lesions & injuries of spinal cord above this level requiring only small enemas given early in the morning, because the core defecation reflex is integrated at conus medularis. </li></ul>
  12. 12. 1 . Absent or abnormal saliva composition can lead to severe premature dental caries in these conditions: <ul><li>A.Sicca syndrome. </li></ul><ul><li>B.Achalasia. </li></ul><ul><li>C. Diabetes mellitus. </li></ul><ul><li>D. Diabetes inspidus. </li></ul><ul><li>E. GERD. </li></ul>
  13. 13. 2 . In Achalasia there is: <ul><li>A. Absent myenteric plexus in esophageal wall. </li></ul><ul><li>B. Defective lower esophageal sphincter. </li></ul><ul><li>C. Defective upper esophageal sphincter. </li></ul><ul><li>D. Failure of LES relaxation during swallowing. </li></ul><ul><li>E. Spastic LES. </li></ul>
  14. 14. 3 . H pylori predisposes to PUD through: <ul><li>A. Decreasing mucosal defensives. </li></ul><ul><li>B. Causing hyperchorhydria. </li></ul><ul><li>C. Hypochlorhydria. </li></ul><ul><li>D. All. </li></ul><ul><li>E. None. </li></ul>
  15. 15. 4 . In Autoimmune gastritis there is: <ul><li>A. Achorhydria. </li></ul><ul><li>B. Absent pepsin. </li></ul><ul><li>C. Protein maldigestion. </li></ul><ul><li>D. Anemia. </li></ul><ul><li>E. Absent gastrin. </li></ul>
  16. 16. 5 . In Autoimmune gastritis there is: <ul><li>A. Achorhydria. </li></ul><ul><li>B. Absent pepsin. </li></ul><ul><li>C. Protein maldigestion. </li></ul><ul><li>D. Anemia. </li></ul><ul><li>E. Absent gastrin. </li></ul>
  17. 17. 6 . Prostaglandins induce ulcer healing by: <ul><li>A. Decreasing acid production. </li></ul><ul><li>B. Increasing acid production. </li></ul><ul><li>C. Enhancing mucosal defenses. </li></ul><ul><li>D. All. </li></ul><ul><li>E. Neither. </li></ul>
  18. 18. 7 . Chemoreceptor trigger zone: <ul><li>A. Is the main vomiting center. </li></ul><ul><li>B. Is a second vomiting center. </li></ul><ul><li>C. Responsible for drug-induced vomiting. </li></ul><ul><li>D. Causes vomiting of pregnancy. </li></ul><ul><li>E. Acts independent of medullary vomiting center. </li></ul>
  19. 19. 8 . Malabsorbtion of nutrients occurs due to: <ul><li>A. Deficiency of saliva. </li></ul><ul><li>B. Deficiency of pancreatic enzymes. </li></ul><ul><li>C. Deficiency of bile. </li></ul><ul><li>D. Deficiency of pepsin. </li></ul><ul><li>E. Colonic diseases. </li></ul>
  20. 20. 9 . Most severe constipation due to spinal cord trauma occur in: <ul><li>A. Lesions in quada equina. </li></ul><ul><li>B. Lesions below cauda equina level. </li></ul><ul><li>C. Lesions above cauda equina level. </li></ul><ul><li>D. All. </li></ul><ul><li>E. None. </li></ul>